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Cardiovascular II > Cardiac Path Robbins Part 1 > Flashcards

Cardiac Path Robbins Part 1 Flashcards

1
Q

cardiac valves- tri-layered architecture

A
  • dense collagenous core (fibrosa) at the outflow surface and connected to the valvular supporting structures
  • central core of loose CT (spongiosa)
  • layer rich in elastin (ventricularis or atrialis) on inflow surface
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2
Q

valves- critical to fxn

A

valvular interstitial cells (most abundant cell type in heart valves)
-syn ECM and express matrix degrading enzymes

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3
Q

pathologic changes to valves- 3 types

A
  • damage to collagen that weakens the leaflets (example- mitral valve prolapse)
  • nodular calcification beginning in interstitial cells (calcific aortic stenosis)
  • fibrotic thickening (rheumatic heart disease)
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4
Q

components of conduction system

A
  • SA node
  • AV node
  • bundle of HIS (connects right atrium to ventricular septum)
  • purkinje network
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5
Q

3 major epicardial coronary a’s

A
  • LAD (left ant descending) and LCX (left circumflex) a’s arise from left coronary a
  • right coronary a
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6
Q

LAD and LCX divisions

A
  • LAD- diagonal branches

- LCX- marginal branches

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7
Q

aging and the heart- myocardium and chambers

A
  • dec LV chamber size (sigmoid septum- bulging of vasal ventricular septum into left ventricular outflow tract)
  • inc epicardial fat
  • myocardial changes:
  • lipofuscin and basophilic degeneration (gray-blue byproduct of glycogen metabolism)
  • fewer myocytes, inc collagen fibers
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8
Q

aging and the heart- valves

A
  • aortic and mitral valve annular calcification
  • fibrous thickening
  • mitral valve leaflets buckling towards left atrium- inc left atrium size
  • lambl excrescences (small filiform processes on the closure lines of aortic and mitral valves- due to small thrombi)
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9
Q

aging and the heart- vascular changes

A
  • coronary atherosclerosis

- stiffening of aorta

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10
Q

cardiovascular dysfxn- 6 principal mech’s

A
  • pump failure
  • flow obstruction
  • regurgitant flow
  • shunted flow
  • disorders of cardiac conduction
  • rupture of the heart or a major vessel
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11
Q

Congestive HF

A

-when heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with inc filling pressure

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12
Q

CHF- result from?

A
  • loss of myocardial contractile fxn (systolic dysfxn)

- loss of ability to fill the ventricles during diastole (diastolic dysfxn)

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13
Q

CHF- mech’s that maintain arterial P and organ perfusion

A
  • Frank-Starling mech- inc filling volumes dilate the heart- inc actin-myosin cross-bridge formation- enhance contractility/SV
  • myocardial adaptations- hypertrophy w/ or w/o cardiac chamber dilation
  • act of neurohumoral systems- NE inc HR, act of renin-ang-aldosterone system, release of ANP
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14
Q

cardiac hypertrophy- caused by

A
  • sustained inc in mechanical work due to P or volume overload
  • trophic signals (B-R’s)
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15
Q

cardiac myocytes become hypertrophic when?

A
  • sustained pressure or volume overload

- sustained trophic signals (B-adrenergic stim)

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16
Q

pressure overload- causes what?

A
  • myocytes become thicker

- left ventricular wall thickness inc concentrically

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17
Q

volume overload- causes what?

A
  • myocytes elongate

- ventricular dilation

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18
Q

cardiac hypertrophy- accompanied by?

A
  • not accompanied by a inc in blood supply

- vulnerable to ischemia-related decompensation

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19
Q

best measure of hypertrophy

A

heart weight (rather than wall thickness)

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20
Q

the molecular/cellular changes in hypertrophied hearts that initially mediate enhanced fxn may contribute to the development of HF- thru?

A
  • abnormal myocardial metabolism
  • alterations of intracellular handling of ca ions
  • myocyte apoptosis
  • reprogramming of gene expression
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21
Q

increases cardiac work, causing hypertrophy

A
  • HTN (p overload)
  • valvular disease (p and or volume overload)
  • MI (volume overload)
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22
Q

CHF- characterized by?

A
  • dec CO and tissue perfusion (forward failure)

- pooling of blood in venous capacitance system (backward failure)- causes pulm edema and/or peripheral edema

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23
Q

left-sided heart failure- most commonly a result of?

A

(can be systolic or diastolic failure)

  • MI
  • HTN
  • left-sided valve disease
  • primary myocardial disease
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24
Q

left-sided heart failure- clinical effects are due to?

A
  • congestion in pulm circulation
  • stasis of blood in left-sided chambers
  • dec tissue perfusion
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25
Q

left-sided heart failure- morphologic changes

A
  • left ventricular hypertrophy
  • left ventricular dysfxn- left atrial dilation (leads to atrial fibrillation, stasis, thrombus)
  • pulm congestion and edema (cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea)
  • heart failure cells (hemosiderin-laden macrophages)- signs of pulm edema!!
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26
Q

left-sided heart failure- dec ejection fraction may result in?

A
  • dec glomerular perfusion- stim release of renin- inc volume- prerenal azotemia
  • dec cerebral perfusion-hypoxic encephalopathy
27
Q

left-sided HF- divided into

A
  • systolic failure- insuff ejection fraction
  • diastolic failure- abnormally stiff and cannot relax during diastole- heart unable to inc its output in response to inc metabolic demands of peripheral tissues- cant expand normally so any inc in filling P goes back to pulm circulation (flash pulm edema)
28
Q

diastolic failure- most common in?

A
  • > 65 age, women
  • HTN- most common cause!!
  • diabetes, obesity, b/l renal a stenosis
29
Q

right-sided heart failure (cor pulmonale)- most common cause is?

A

-left-sided failure!!

30
Q

isolated right-sided HF- results from?

A

any cause of pulm HTN!!!!

  • parenchymal lung diseases
  • primary pulm HTN
  • pulm vasoconstriction
31
Q

primary right-sided HF

A
  • pulm congestion is minimal
  • venous system is markedly congested: liver congestion, splenic congestion, effusions in peritoneal, pleural, pericardial spaces, edema, renal congestion
32
Q

right-sided HF- morphology

A
  • congestive hepatomegaly- red/brown pericentral zones- “nutmeg liver”
  • centrilobular necrosis- when left-sided HF w/ hypoperfusion is present
  • cardiac cirrhosis- longstanding HF
  • congestive splenomegaly
  • effusions in peritoneal, pleural and pericardial spaces
  • edema of peripheral and dependent portions of body (ankles)- hallmark!!
  • generalized edema may occur (anasarca)
33
Q

ischemic heart disease- may result in?

A
  • MI
  • angina pectoris
  • chronic ischemic heart disease, with HF
  • sudden cardiac death
34
Q

leading cause of death in US?

A

ischemic heart disease (90% secondary to atherosclerosis)

  • chronic vascular occlusion
  • acute plaque change- thrombus
35
Q

most common type of pediatric heart disease

A

-congenital CV malformations

36
Q

1st and 2nd heart fields- express?

A
  • 1st heart field- Hand1 TF

- 2nd heart field- Hand2 and GF-10

37
Q

1st and 2nd heart field- becomes?

A
  • 1st heart field- left ventricle

- 2nd heart field- outflow tract, right ventricle, atria

38
Q

2 critical events that occur by day 28

A

(when initial cell crescent develops into a beat in tube- loops to right and begins to form the basic heart chambers 8 days later)

  • neural crest-derived cells migrate into the outflow tract- participate in the septation of the outflow tract and the formation of the aortic arches
  • interstitial CT that will become the AV canal and outflow tract enlarges to produce endocardial cushings
39
Q

proper development of heart- depends on what TFs?

A

-Wnt, hedgehog, VEGF, bone morphogenetic factor, TGFB, fibroblast GF, Notch pathways

40
Q

development of heart- day 15

A

-first heart field (FHF) cells form a crescent shape in the ant embryo with second heart field (SHF) cells

41
Q

development of heart- day 21

A

-SHF cells lie dorsal to the straight heart tube, begin to migrate into the ant and posterior ends of the tube to from the right ventricle, conotruncus , and part of atria

42
Q

development of heart- day 28

A

-cardiac neural crest cells migrate into the outflow tract from the neural folds to septate the outflow tract and pattern the bilaterally symmetric aortic arch a’s

43
Q

development of heart- day 50

A

-septation of ventricles, atria, and AV valves results in the 4-chambered heart

44
Q

major known cause of congenital heart disease

A

sporadic genetic abnormalities

45
Q

3 TFs that are mutated in some pts with atrial and ventricular septal defects

A
  • GATA4, TBX5, NKX2-5

- bind together and co-reg the expression of target genes

46
Q

deletion of chromosome 22q11.2- what syndrome?

A

(50% of pts with DiGeorge syndrome)

  • 4th branchial arch and derivatives of the 3rd and 4th pharyngeal pouches (formation of thymus, parathyroids, heart) develop abnormally
  • CATCH-22- cardiac abnormality, abnormal facies, thymic aplasia, cleft palate, hypocalcemia; all on chrom 22!
  • due to deletion of TBX1 (reg neural crest migration)
47
Q

most common genetic cause of congenital heart disease is?

A
  • trisomy 21 (down syndrome)- 40% of pts have heart defect

- most often involves structures form second hart field

48
Q

congenital heart disease- structural abnormalities divided into 3 categories

A
  • left-to-right shunt
  • right-to-left shunt
  • obstruction
49
Q

shunt- is what?

A

abnormal communication b.w chambers or BVs

50
Q

right-to-left shunt

A
  • hypoxia and cyanosis results (pulm circulation is bypassed)
  • allow emboli from peripheral v’s to bypass the lungs and go into systemic circulation (paradoxical embolism)
  • long standing cyanosis causes -hypertrophic osteoarthropathy (clubbing of fingers/toes) and polycythemia
51
Q

most important causes of right-to-left shunt

A
  • Tetralogy of Fallot
  • transposition of great a’s
  • persistent truncus arteriosus
  • tricuspid atresia
  • total anomalous pulm venous connection
52
Q

left-to-right shunts

A
  • inc pulmonary blood flow (but are not initially assoc with cyanosis)
  • elevate volume and P in the normally low-P pulm circulation
  • muscular pulm a’s respond by medial hypertrophy and vasoconstriction- causes obstructive intimal lesions
  • right ventricle hypertrophy
  • eventually, pulm vascular resistance approaches systemic levels, so becomes a right-to-left shunt (Eisenmenger syndrome)
53
Q

obstructive congenital heart disease

A

-complete obstrudction- atresia

54
Q

left-to-right shunts; includes?

A
  • most common congenital heart disease
  • ASD (atrial septal defect)
  • VSD (ventricular septal defect)
  • PDA (patent ductus arteriosus)
55
Q

atrial septal defect

A
  • caused by incomplete tissue formation- allows communication of blood b/w left and right atria
  • usually asymptomatic until adulthood
  • shouldnt be confused with PFO (patent foramen ovale)
56
Q



ASD and PFO- defects in the formation of interatrial septum- developmental stages of this structure:

A
  • septum primum- partially separates the atria (anterior opening- ostium primum)
  • septum primum develops a second posterior opening- ostium secundum (septum secundum- ingrowth to right and anterior of septum primum)
  • foramen ovale is continuous with the ostium secundum
  • septum secundum enlarges until it forms a flap of tissue that covers the foramen ovale- which closes in response to P gradients b/w atria
57
Q

septum secundum and foramen ovale- what happens in fetal life and at birth?

A
  • valve opens only when the P is greater in the right atrium
  • in fetal life- lungs nonfxnal so the P in pulm circulation is greater than systemic circulation P- so the valve of the foramen ovale is open!!
  • at birth- lungs expand- pulm vascular P’s drop- so rt atrial Ps drop below the left atrium P- foramen ovale closes!
58
Q

ASDs- morphology

A
  • secundum ASD (90%)- deficient formation near the center of the atrial septum; not assoc with other anomalies
  • primum anomalies (5%)- occur adj to AV valves, often assoc with AV valve abnormalities and a VSD
  • sinus venous defects (5%)- near the entrance of SVC- assoc with anomalous pulm venous return to rt atrium
59
Q

ASDS- clinical features

A
  • left-to-right shunt (b/c systemic vascular R > pulm vascular R and right ventricle compliance is greater than the left)
  • pulm blood flow 2-8x more than normal
  • murmur due to flow thru the pulm valve and ASD
  • well tolerated!
  • not symptomatic until age 30
  • low mortality
60
Q

patent foramen ovale

A
  • closes in 80% of ppl by 2 yrs of age
  • unsealed flap can open if right-sided P’s become elevated
  • sustained pulm HTN or transient (sneeze, cough)- could cause a paradoxical embolism due to right-to-left shunting
61
Q

Ventricular septal defect- morphology

A
  • most common form of congenital heart disease
  • 90%- membranous VSD- occur in the region of membranous interventricular septum
  • remainder- infundibular VSD- below the pulm valve or within the muscular septum
62
Q

VSD- clinical features

A
  • most that manifest in kids are assoc with other cardiac anomalies (Tertralogy of Fallot)
  • if first detected in an adult- usually an isolated defect!
  • 50% of small VSDs close spontaneously
  • large defects cause left-to-right shunting- right ventricular hypertrophy and pulm HTN!- can reverse flow thru shunt- cyanosis!!
63
Q

patent ductus arteriosus

A
  • arises from pulm aorta and joins the aorta
  • in fetus life- permits blood flow from pulm a to aorta (bypasses the unoxygenated lungs)
  • after birth- closes in 1-2 days (due to dec pulm vascular R, dec PGE2)
  • closes- forms ligamentum arteriosum
  • ductal closure delayed in infants with hypoxia or when PDA occurs in assoc with other defects (VSDs that inc Pulm vascular P’s)
64
Q

patent ductus arteriosus- clinical

A
  • harsh “machinery-like” murmur
  • usually asymptomatic at birth
  • no cyanosis b/c the shunt is initially left-to-right
  • should close it as early in life as possible!!
  • keeping it open may save infants with other malformations

Cardiovascular II (13 decks)

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